Recent reports of prion disease developing in four dairy farmers and two teenagers in Britain have raised renewed concerns about the potential health risk of bovine spongiform encephalopathy to humans. Documented transmission of bovine spongiform encephalopathy to non-human primates indicates that such concerns are not without foundation.1 Although prions are not conventional pathogens, many of the basic principles governing microbial pathogenesis seem to apply to the infectious forms of prion diseases. In this context human risk of infection after exposure to bovine spongiform encephalopathy can be considered in terms of the size of the infecting inoculum, the potential routes of entry into the host, and factors of host susceptibility.